PAIN DRUGS HANDBOOK TABLE
OF CONTENTS
About the
Author
About
the Handbook
Acknowledgments
Forward
to 2rd Edition
Forward
to 1st Edition
DRUGS (Alphabetical Order)
TOPICAL AGENTS
Amitriptyline
Baclofen
Clonidine
Cyclobenzaprine
2-deoxy-d-glucose
Dexamethasone
Dextromethorphan
Diclofenac
Doxepin
DMSO
Gabapentin
Ketamine
Ketoprofen
NEUROLYTIC AGENT
Phenol
APPENDICES
Appendix 1: World Health Organization
Three-step Ladder
Appendix 2: Drug Tables
Appendix 3: Infusion Tables
Appendix 4: Relative Potencies of
Opioids Effects
Appendix 5: Relative Potencies of Steroids
Appendix 6: Intravenous PCA
Standard Orders
Appendix 7: Patient Controlled Analgesia Flow Sheet
Appendix 8: Relative Potencies of Opioids
Appendix 9: Epidural Analgesia Monitoring Orders
Appendix 10: Pain Rating Scales
Appendix 11: Multiplication Factors for Converting the
Daily Dose of a Prior Opioid to the Daily Dose of Oxycontin
Appendix 12: CPR Algorithms
Appendix 13: Pediatric CPR Algorithms
Appendix 14: Trade Name Table
BIBLIOGRAPHY
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Sota
Omoigui's
Pain Drug Handbook
2nd Edition:
Ketoprofen
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SECTION
ONE:
Class,
Uses, Dosing,
Elimination
SECTION TWO:
Preparation, Pharmacology, Pharmacokinetics
SECTION THREE:
Interactions, Toxicity
Guidelines/Precautions
Principal Adverse Reactions
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Class
(NONSTEROIDAL ANTI-INFLAMMATORY AGENT)
Uses
symptomatic treatment of mild to moderate inflammatory and degenerative arthritis, primary dysmenorrhea, tension headache, post-operative and post- traumatic pain, chronic pain, cancer pain (especially with bone metastasis).
Dosing
Pain : Ketoprofen: PO 25 -50 mg (0.5-1 mg/kg) every six to eight hours. Max. dose 300 mg daily
Ketoprofen (extended release): PO 200 mg once daily at bedtime
Inflammatory Disease : Ketoprofen: PO 50-75 mg (1-1.5 mg/kg) every six to eight hours. Max. dose 300 mg daily
Ketoprofen (extended release): PO 200 mg once daily at bedtime
Patients with rheumatoid or acute gouty arthritis may require larger doses than those with osteoarthritis.
Administer analgesic regularly (not prn). Addition of opioid analgesics, antidepressant agents and use of non-drug therapies e.g. TENS may enhance analgesia (see front matter for drug combinations). In rheumatoid arthritis or juvenile rheumatoid arthritis, second line rheumatoid agents may include leflunomide (arava), etanercept (enbrel), antimalarials or methotrexate. In geriatric patients, and patients with decreased renal or hepatic function, decrease doses by one-third to one-half. Incidence of Ketoprofen induced gastropathy may be decreased by administration with meals, milk, antacids or sucralfate (PO 1 gram qid). Misoprostol (PO 100-200 mcg qid) may be used to prevent gastric ulcers in high-risk patients.
Elimination
hepatic, renal.
Preparation
Ketoprofen (Orudis)
Oral Capsules: 25 mg, 50 mg, 75 mg
Ketoprofen - non prescription (Orudis KT, Actron)
Oral Caplets: 12.5 mg,
Oral Tablets: 12.5 mg
Ketoprofen (Oruvail)
Oral Capsules, extended release: 200 mg
Pharmacology
A propionic derivative and nonsteroidal anti-inflammatory drug (NSAID) , Ketoprofen is structurally and pharmacologically related to ibuprofen and naproxen. Like other NSAIDs, the analgesic and anti-inflammatory activities of Ketoprofen are partly due to the inhibition of prostaglandin and leukotriene synthesis, antibradykinin and lysosomal membrane stabilizing activity . The antipyretic activity of Ketoprofen may occur secondary to inhibition of pyrogen induced release of prostaglandins in the central nervous system (including the hypothalamus) and possibly to centrally mediated peripheral vasodilation. Analgesic potency of ketoprofen is similar to that of indomethacin and about 20 times that of ibuprofen or aspirin. Ketoprofen (like other NSAIDs) exhibits a ceiling effect for analgesia. Exceeding recommended doses results in increased toxicity without improvement in analgesia. Ketoprofen may cause gastric mucosal damage which may result in ulceration or bleeding. Inhibition of prostaglandin synthesis may result in decreased uterine tone, contractility and prolonged gestation in the parturient and premature closure of the ductus arteriosus in the fetus. Ketoprofen inhibits platelet aggregation and prolongs bleeding time (to a greater extent than indomethacin). However, unlike the irreversible effects of aspirin, these effects are transient and platelet function and aggregation return to normal within 24 hours. The drug has no uricosuric activity.
Pharmacokinetics
ONSET OF ACTION: PO: analgesic effect 15-30 minutes
PEAK EFFECT: PO: analgesic effect 1-2 hours
DURATION OF ACTION: PO: analgesic effect 3-4 hours
Interactions
risks of bleeding increased with concomitant NSAIDs, anticoagulant or heparin therapy, alcohol ingestion; decreases antihypertensive effects of beta adrenergic blocking agents; serum levels of Ketoprofen decreased or increased by concomitant aspirin; serum levels of Ketoprofen increased by concomitant probenecid; serum levels and toxic effects of methotrexate, lithium increased by concomitant ketoprofen; GI absorption of ketoprofen delayed by food and milk; prostaglandin mediated natriuretic effects of loop diuretics antagonized by ketoprofen.
Toxicity
Toxic Range:
Not routinely monitored
Manifestations:
Acute - drowsiness, vomiting, abdominal pain, metabolic acidosis
Antidote:
None
Management:
Discontinue or reduce medication
Correction of fluid, electrolyte and acid-base disturbances
Support ventilation and circulation (Patent Airway, Oxygen, IV Fluids, Vasopressors)
Airway protected - ipecac syrup induced emesis (30 mls or 0.5 mls/kg ipecac syrup followed by 200 mls or 4 mls/kg of water or clear fluid) or gastric lavage (with drug ingestion) followed by administration of activated charcoal (PO 50-100 grams or 1-2 gram/kg)
Forced alkaline diuresis with IV sodium bicarbonate (IV furosemide if necessary) after correction of dehydration.
Hemodialysis
Symptomatic treatment
Guidelines
(1) Use with caution in patients with active GI lesions (e.g. erosive gastritis, peptic ulcer), a history of recurrent GI lesions, hepatic/renal dysfunction, preexisting hypoprothrombinemia and vitamin K deficiency. Ketoprofen may cause peripheral edema and should also be used cautiously in patients with heart failure, hypertension and other conditions associated with fluid retention.
(2) Renal prostaglandins may have a supportive role in maintaining renal perfusion in patients with pre-renal conditions. Ketoprofen should be avoided in such patients as it may cause a dose-dependent decrease in prostaglandin formation and thus precipitate renal decompensation
(3) Observe carefully patients with coagulation disorders and those receiving drug therapy that interferes with hemostasis.
(4) Use with caution in pregnancy and only when the perceived benefits outweigh the risks.
(5) Patient response to NSAIDs is variable. Patients who do not respond to or cannot tolerate ketoprofen may be successfully treated with another NSAID.
(6) Ketoprofen and salicylates should not be administered concomitantly because there may not be any therapeutic advantage and incidences of adverse GI side effects may be increased.
(7) Contraindicated in patients with previously demonstrated hypersensitivity to Ketoprofen or with the complete or partial syndrome of nasal polyps, angioedema or bronchospastic reactivity to aspirin or other nonsteroidal anti-inflammatory drugs (NSAID).
(8) Signs and symptoms of infection or other diseases may be masked by the antipyretic and anti-inflammatory effects of Ketoprofen.
(9) Monitor stool for blood every 14 days, and BUN, serum creatinine, urinanalysis every 1-2 months when the drug administered at chronic high doses.
Adverse
CVS: peripheral edema, fluid retention, hypertension, palpitation
PULM: dyspnea, bronchospasm
CNS: drowsiness, dizziness, headache, anxiety, confusion
GI: ulceration, bleeding, dyspepsia, nausea, vomiting, diarrhea, hepatic dysfunction
GU: renal dysfunction, acute renal failure, azotemia, cystitis, hematuria,
DERM: pruritus, urticaria
HEMATOLOGIC: prolongation of bleeding time, leukopenia, thrombocytopenia, aplastic anemia, hemolytic anemia
OTHER: tinnitus, blurred vision
Reactions
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